# In vitro and in vivo efficacy of aurintricarboxylic acid against Neospora caninum infection : Efficacy of aurintricarboxylic acid against N. caninum infection

**Authors:** Zhengkai Wei, Yuxiao Qian, Xi Jiang, Yuqian Jiang, Rongsheng Huang, Kaifeng He, Jing Huang, Jiaxuan Wang, Xin Guo, Wenlong Huang, Dezhi Zhang, Zhengtao Yang, Quan Liu, Qianyong Li

PMC · DOI: 10.3724/abbs.2025006 · Acta Biochimica et Biophysica Sinica · 2025-03-28

## TL;DR

This study shows that aurintricarboxylic acid (ATA) can effectively fight Neospora caninum, a parasite that causes bovine neosporosis, both in lab tests and in mice.

## Contribution

The study is the first to demonstrate the anti-Neospora caninum efficacy of aurintricarboxylic acid.

## Key findings

- ATA inhibits Neospora caninum proliferation and reduces parasite loads in cells.
- ATA disrupts the parasite's ultrastructure and modulates immune responses by downregulating key cytokines.
- In mice, ATA reduces parasite loads in organs and improves body weight and pathology.

## Abstract

Bovine neosporosis, a protozoal disease caused by
Neospora caninum (
N.
caninum), poses a significant threat to the global cattle industry, resulting in substantial economic losses that are difficult to quantify. The current lack of effective commercial vaccines and specific treatments highlights the urgent need for the development of potent drugs against
N.
caninum. In this study, we investigate the efficacy of aurintricarboxylic acid (ATA), a derivative of polyaromatic carboxylic acid, against
N.
caninum both
in vitro and
in vivo. Cell cytotoxicity is evaluated using CCK-8 kits.
N.
caninum proliferation within cells is assessed by qPCR analysis. Transmission electron microscopy (TEM) is employed to examine the ultrastructures of
N.
caninum tachyzoites. The efficacy of ATA against
N.
caninum infection is validated in a mouse model. Our findings indicate that ATA not only inhibits
N.
caninum proliferation but also reduces parasite loads within individual cells. Furthermore, ATA (20 and 40 μM) has immunomodulatory effects by downregulating the mRNA expressions of
N.
caninum-induced cytokines, including tumor necrosis factor-α (TNF-α), interferon (IFN-α, -β, and -γ), and β-defensin 5 (BNBD5). ATA treatment directly targets and eliminates
N.
caninum by disrupting its ultrastructure. The
in vivo study confirms the potential of ATA to increase body weight, decrease parasite loads in the lungs and duodenum, and ameliorate the pathological effects induced by
N.
caninum infection in mice. In conclusion, this study represents the first evidence of the anti-
N.
caninum ability of ATA and provides compelling data to support its potential as a candidate for developing anti-
N.
caninum drugs.

## Linked entities

- **Chemicals:** aurintricarboxylic acid (PubChem CID 2259)
- **Species:** Neospora caninum (taxon 29176), Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** caninum infection (MESH:D007239), protozoal disease (MESH:D020808), cytotoxicity (MESH:D064420)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Neospora caninum (species) [taxon 29176], Bos taurus (bovine, species) [taxon 9913]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12536456/full.md

## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12536456/full.md

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Source: https://tomesphere.com/paper/PMC12536456